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Chronic Rhinosinusitis (CRS) defines a group of upper airway disorders characterized by persistent inflammation of the sinonasal cavities. Depending on the presence of polyps on endoscopic examination, CRS can be further divided into 2 groups: CRS without nasal polyps (CRSsNP) and CRS with nasal polyps (CRSwNP). Typically, CRSwNP is closely related to eosinophilic and Th2-related inflammation while in CRSsNP neutrophils dominate the infiltrate. Secretory IgA (SIgA) represents a first-line mechanism of the airway immune defense, protecting the mucosal surfaces against inhaled microorganisms and antigens. Epithelial transcytosis of IgA is mediated by the polymeric immunoglobulin receptor (pIgR), a transmembrane glycoprotein selectively expressed on the basolateral surface of epithelial cells which also serves as the precursor of secretory component (SC), a glycoprotein that enhances the immune functions of SIgA. One previous report indicated that Igs, including IgA, were increased in tissue homogenates from patients with CRSwNP (Van Zele, 2006). Our laboratory has identified in the bronchial epithelium of severe COPD decreases in pIgR and IgA expression (Pilette, 2001) and related these findings to airflow limitation and neutrophilic inflammation (Pilette, 2001, 2007). Based on this and on the role of IgA in mucosal host defense, as well as clinical evidence suggesting deficient first-line defense mechanisms, we hypothesized that secretory IgA production could be impaired in CRSsNP, considered as the upper airway counterpart of COPD.
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Hupin, C., Lecocq, M., Rombaux, P., & Pilette, C. (2012). Downregulation of pIgR Expression in Patients with CRSwNP. European Academy of Allergy and Clinical Immunology Congress 2012 (EAACI), Genève, Suisse. https://hdl.handle.net/2078.5/45776